@article{MTMT:32266554,
	title = {Olaparib : A Clinically Applied PARP Inhibitor Protects from Experimental Crohn's Disease and Maintains Barrier Integrity by Improving Bioenergetics through Rescuing Glycolysis in Colonic Epithelial Cells},
	url = {https://m2.mtmt.hu/api/publication/32266554},
	author = {Kovács, Dominika and Bagóné Vántus, Viola and Vámos, Eszter and Kálmán, Nikoletta and Schicho, Rudolf and Gallyas, Ferenc and Radnai, Balázs},
	doi = {10.1155/2021/7308897},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2021},
	unique-id = {32266554},
	issn = {1942-0900},
	abstract = {Crohn's disease (CD) is an inflammatory disorder of the intestines characterized by epithelial barrier dysfunction and mucosal damage. The activity of poly(ADP-ribose) polymerase-1 (PARP-1) is deeply involved in the pathomechanism of inflammation since it leads to energy depletion and mitochondrial failure in cells. Focusing on the epithelial barrier integrity and bioenergetics of epithelial cells, we investigated whether the clinically applied PARP inhibitor olaparib might improve experimental CD. We used the oral PARP inhibitor olaparib in the 2,4,6-trinitrobenzene sulfonic acid- (TNBS-) induced mouse colitis model. Inflammatory scoring, cytokine levels, colon histology, hematological analysis, and intestinal permeability were studied. Caco-2 monolayer culture was utilized as an epithelial barrier model, on which we used qPCR and light microscopy imaging, and measured impedance-based barrier integrity, FITC-dextran permeability, apoptosis, mitochondrial oxygen consumption rate, and extracellular acidification rate. Olaparib reduced the inflammation score, the concentration of IL-1β and IL-6, enhanced the level of IL-10, and decreased the intestinal permeability in TNBS-colitis. Blood cell ratios, such as lymphocyte to monocyte ratio, platelet to lymphocyte ratio, and neutrophil to lymphocyte ratio were improved. In H2O2-treated Caco-2 monolayer, olaparib decreased morphological changes, barrier permeability, and preserved barrier integrity. In oxidative stress, olaparib enhanced glycolysis (extracellular acidification rate), and it improved mitochondrial function (mitochondrial coupling efficiency, maximal respiration, and spare respiratory capacity) in epithelial cells. Olaparib, a PARP inhibitor used in human cancer therapy, improved experimental CD and protected intestinal barrier integrity by preventing its energetic collapse; therefore, it could be repurposed for the therapy of Crohn's disease.},
	year = {2021},
	eissn = {1942-0994},
	orcid-numbers = {Vámos, Eszter/0000-0003-0622-442X; Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:32113887,
	title = {Syntheses and Study of a Pyrroline Nitroxide Condensed Phospholene Oxide and a Pyrroline Nitroxide Attached Diphenylphosphine},
	url = {https://m2.mtmt.hu/api/publication/32113887},
	author = {Isbera, Mostafa and Bognár, Balázs and Gallyas, Ferenc and Bényei, Attila Csaba and Jekő, József and Kálai, Tamás},
	doi = {10.3390/molecules26144366},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {26},
	unique-id = {32113887},
	issn = {1420-3049},
	abstract = {The reaction of a diene nitroxide precursor with dichlorophenylphosphine in a McCormac procedure afforded 1,1,3,3-tetramethyl-5-phenyl-1,2,3,4,5,6-hexahydrophospholo[3,4-c]pyrrole-5-oxide-2-oxyl. Lithiation of the protected 3-iodo-pyrroline nitroxide followed by treatment with chlorodiphenylphosphine after deprotection afforded (1-oxyl-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)diphenylphosphine oxide, and after reduction, (1-oxyl-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)diphenylphosphine was realized, which was also supported by X-ray single crystal diffraction measurements. This pyrroline diphenylphosphine derivative was converted to hexadecylphosphonium salt, which is an analogue of antineoplastic agent, MITO-CP.},
	keywords = {REDUCTION; NITROXIDES; protecting groups; Lithiation; McCormac reaction},
	year = {2021},
	eissn = {1420-3049},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:31997390,
	title = {Microarray-predicted molecular effect of WT1 isoforms in MCF-7 breast cancer cell line},
	url = {https://m2.mtmt.hu/api/publication/31997390},
	author = {Kanokwiroon, K. and Erős, Krisztián and Graidist, P. and Nakatake, A. and Morishita, K.},
	journal-iso = {FEBS OPEN BIO},
	journal = {FEBS OPEN BIO},
	volume = {9},
	unique-id = {31997390},
	issn = {2211-5463},
	year = {2019},
	eissn = {2211-5463},
	pages = {333-333}
}

@article{MTMT:30356192,
	title = {Introduction},
	url = {https://m2.mtmt.hu/api/publication/30356192},
	author = {Bock-Marquette, Ildikó and Gallyas, Ferenc},
	doi = {10.1139/cjpp-2018-0484},
	journal-iso = {CAN J PHYSIOL PHARM},
	journal = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
	volume = {96},
	unique-id = {30356192},
	issn = {0008-4212},
	year = {2018},
	eissn = {1205-7541},
	pages = {V-V},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:3422217,
	title = {The effect of serum triglyceride concentration on the outcome of acute pancreatitis : systematic review and meta-analysis},
	url = {https://m2.mtmt.hu/api/publication/3422217},
	author = {Kiss, Lóránd and Fűr, Gabriella and Mátrai, Péter and Hegyi, Péter and Ivány, Emese and Cazacu, IM and Szabó, Imre and Habon, Tamás and Alizadeh, Hussain and Gyöngyi, Zoltán and Vigh, Éva and Erőss, Bálint Mihály and Erős, Adrienn and Ottoffy, M and Czakó, László and Rakonczay, Zoltán},
	doi = {10.1038/s41598-018-32337-x},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {8},
	unique-id = {3422217},
	issn = {2045-2322},
	abstract = {Elevated serum triglyceride concentration (seTG, >1.7 mM or >150 mg/dL) or in other words hypertriglyceridemia (HTG) is common in the populations of developed countries. This condition is accompanied by an increased risk for various diseases, such as acute pancreatitis (AP). It has been proposed that HTG could also worsen the course of AP. Therefore, in this meta-analysis, we aimed to compare the effects of various seTGs on the severity, mortality, local and systemic complications of AP, and on intensive care unit admission. 16 eligible studies, including 11,965 patients were retrieved from PubMed and Embase. The results showed that HTG significantly elevated the odds ratio (OR = 1.72) for severe AP when compared to patients with normal seTG (<1.7 mM). Furthermore, a significantly higher occurrence of pancreatic necrosis, persistent organ failure and renal failure was observed in groups with HTG. The rates of complications and mortality for AP were significantly increased in patients with seTG >5.6 mM or >11.3 mM versus <5.6 mM or <11.3 mM, respectively. We conclude that the presence of HTG worsens the course and outcome of AP, but we found no significant difference in AP severity based on the extent of HTG.},
	keywords = {[Meta-analysis]},
	year = {2018},
	eissn = {2045-2322},
	orcid-numbers = {Hegyi, Péter/0000-0003-0399-7259; Habon, Tamás/0000-0002-4816-857X; Gyöngyi, Zoltán/0000-0001-9330-9119; Erőss, Bálint Mihály/0000-0003-3658-8427; Czakó, László/0000-0002-6331-0802; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:3407190,
	title = {Orthologous proteins of experimental de- and remyelination are differentially regulated in the CSF proteome of multiple sclerosis subtypes},
	url = {https://m2.mtmt.hu/api/publication/3407190},
	author = {Martin, NA and Nawrocki, A and Molnár, Viktor and Elkjaer, ML and Thygesen, EK and Palkovits, Miklós and Ács, Péter and Sejbaek, T and Nielsen, HH and Hegedűs, Zoltán and Sellebjerg, F and Molnár, Tihamér and Barbosa, EGV and Alcaraz, N and Gallyas, Ferenc and Svenningsen, AF and Baumbach, J and Lassmann, H and Larsen, MR and Illés, Zsolt László},
	doi = {10.1371/journal.pone.0202530},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {13},
	unique-id = {3407190},
	issn = {1932-6203},
	abstract = {OBJECTIVE: Here, we applied a multi-omics approach (i) to examine molecular pathways related to de- and remyelination in multiple sclerosis (MS) lesions; and (ii) to translate these findings to the CSF proteome in order to identify molecules that are differentially expressed among MS subtypes. METHODS: To relate differentially expressed genes in MS lesions to de- and remyelination, we compared transcriptome of MS lesions to transcriptome of cuprizone (CPZ)-induced de- and remyelination. Protein products of the overlapping orthologous genes were measured within the CSF by quantitative proteomics, parallel reaction monitoring (PRM). Differentially regulated proteins were correlated with molecular markers of inflammation by using MesoScale multiplex immunoassay. Expression kinetics of differentially regulated orthologous genes and proteins were examined in the CPZ model. RESULTS: In the demyelinated and remyelinated corpus callosum, we detected 1239 differentially expressed genes; 91 orthologues were also differentially expressed in MS lesions. Pathway analysis of these orthologues suggested that the TYROBP (DAP12)-TREM2 pathway, TNF-receptor 1, CYBA and the proteasome subunit PSMB9 were related to de- and remyelination. We designed 129 peptides representing 51 orthologous proteins, measured them by PRM in 97 individual CSF, and compared their levels between relapsing (n = 40) and progressive MS (n = 57). Four proteins were differentially regulated among relapsing and progressive MS: tyrosine protein kinase receptor UFO (UFO), TIMP-1, apolipoprotein C-II (APOC2), and beta-2-microglobulin (B2M). The orthologous genes/proteins in the mouse brain peaked during acute remyelination. UFO, TIMP-1 and B2M levels correlated inversely with inflammation in the CSF (IL-6, MCP-1/CCL2, TARC/CCL17). APOC2 showed positive correlation with IL-2, IL-16 and eotaxin-3/CCL26. CONCLUSIONS: Pathology-based multi-omics identified four CSF markers that were differentially expressed in MS subtypes. Upregulated TIMP-1, UFO and B2M orthologues in relapsing MS were associated with reduced inflammation and reflected reparatory processes, in contrast to the upregulated orthologue APOC2 in progressive MS that reflected changes in lipid metabolism associated with increased inflammation.},
	year = {2018},
	eissn = {1932-6203},
	orcid-numbers = {Molnár, Viktor/0000-0002-4156-9987; Palkovits, Miklós/0000-0003-0578-0387; Gallyas, Ferenc/0000-0002-1906-4333; Illés, Zsolt László/0000-0001-9655-0450}
}

@article{MTMT:3390792,
	title = {The effect of serum triglyceride concentration on the outcome of acute pancreatitis: Systematic review and meta-analysis},
	url = {https://m2.mtmt.hu/api/publication/3390792},
	author = {Kiss, Lóránd and Fűr, Gabriella and Mátrai, Péter and Hegyi, Péter and Ivány, Emese and Mihaela Cazacu, Irina and Szabó, Imre and Habon, Tamás and Alizadeh, Hussain and Gyöngyi, Zoltán and Vigh, Éva and Erőss, Bálint and Erős, Adrienn and Ottoffy, Máté and Czakó, László and Rakonczay, Zoltán},
	doi = {10.1016/j.pan.2018.05.262},
	journal-iso = {PANCREATOLOGY},
	journal = {PANCREATOLOGY},
	volume = {18},
	unique-id = {3390792},
	issn = {1424-3903},
	year = {2018},
	eissn = {1424-3911},
	pages = {S97-S98},
	orcid-numbers = {Hegyi, Péter/0000-0003-0399-7259; Habon, Tamás/0000-0002-4816-857X; Czakó, László/0000-0002-6331-0802; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:3375670,
	title = {Amiodarone’s major metabolite, desethylamiodarone induces apoptosis in human cervical cancer cells},
	url = {https://m2.mtmt.hu/api/publication/3375670},
	author = {Bognár, Zita and Fekete, Katalin and Bognár, Rita and Szabó, Aliz and Vass, Réka Anna and Sümegi, Balázs},
	doi = {10.1139/cjpp-2018-0113},
	journal-iso = {CAN J PHYSIOL PHARM},
	journal = {CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY},
	volume = {96},
	unique-id = {3375670},
	issn = {0008-4212},
	abstract = {Previously, we found that desethylamiodarone (DEA) may have therapeutic potentiality in bladder cancer. In this study, we determined its effects on human cervical cancer cells (HeLa). Cell viability was evaluated by Muse Cell Count & Viability Assay; cell apoptosis was detected by Muse Annexin V & Dead Cell Assay. Cell cycle was flow cytometrically determined by Muse Cell Cycle Kit and the morphological changes of the cells were observed under a fluorescence microscope after Hoechst 33342 staining. The changes in the expression levels of apoptosis-related proteins in the HeLa cells were assessed by immunoblot. Our results showed that DEA significantly inhibited the proliferation and viability of HeLa cells and induced apoptosis in vitro in dose-dependent and also in cell cycle-dependent manner because DEA induced G0/G1 phase arrest in the HeLa cell line. We found that DEA treatment downregulated the expression of phospho-Akt and phospho-Bad. In addition, DEA could downregulate expression of Bcl-2, upregulate Bax, and induce cytochrome c release. Our results indicate that DEA might have significance as an anti-tumor agent against human cervical cancer.},
	keywords = {PHARMACOKINETICS; INHIBITION; APOPTOSIS; ACTIVATION; SURVIVAL; PATHWAY; KINASE; DEATH; Therapy; AKT; Cervical cancer; desethylamiodarone; PI3K-Akt pathway; Bax/Bcl-2; Pharmacology & Pharmacy},
	year = {2018},
	eissn = {1205-7541},
	pages = {1004-1011},
	orcid-numbers = {Vass, Réka Anna/0000-0002-0436-4261}
}

@article{MTMT:3352238,
	title = {Experimental demyelination and axonal loss are reduced in MicroRNA-146a deficient mice},
	url = {https://m2.mtmt.hu/api/publication/3352238},
	author = {Martin, NA and Molnár, Viktor and Szilágyi, Tamás Gábor and Elkjaer, ML and Nawrocki, A and Okarmus, J and Wlodarczyk, A and Thygesen, EK and Palkovits, Miklós and Gallyas, Ferenc and Larsen, MR and Lassmann, H and Benedikz, E and Owens, T and Svenningsen, AF and Illés, Zsolt László},
	doi = {10.3389/fimmu.2018.00490},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {9},
	unique-id = {3352238},
	issn = {1664-3224},
	year = {2018},
	eissn = {1664-3224},
	orcid-numbers = {Molnár, Viktor/0000-0002-4156-9987; Palkovits, Miklós/0000-0003-0578-0387; Gallyas, Ferenc/0000-0002-1906-4333; Illés, Zsolt László/0000-0001-9655-0450}
}

@article{MTMT:3338655,
	title = {The Neurokinin-1 Receptor Contributes to the Early Phase of Lipopolysaccharide-Induced Fever via Stimulation of Peripheral Cyclooxygenase-2 Protein Expression in Mice},
	url = {https://m2.mtmt.hu/api/publication/3338655},
	author = {Pákai, Eszter and Tékus, Valéria and Zsiboras, C and Rumbus, Zoltán and Pótóné Oláh, Emőke and Kéringer, Patrik and Khidhir, N and Mátics, Róbert and Deres, László and Takács-Ördög, Katalin and Szentes, Nikolett and Pohóczky, Krisztina and Kemény, Ágnes and Hegyi, Péter and Pintér, Erika and Garami, András},
	doi = {10.3389/fimmu.2018.00166},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {9},
	unique-id = {3338655},
	issn = {1664-3224},
	year = {2018},
	eissn = {1664-3224},
	orcid-numbers = {Pohóczky, Krisztina/0000-0003-0385-5162; Kemény, Ágnes/0000-0002-4523-3938; Hegyi, Péter/0000-0003-0399-7259; Pintér, Erika/0000-0001-9898-632X; Garami, András/0000-0003-2493-0571}
}